title: The association of near infrared spectroscopy-derived StO2 measurements and biomarkers of endothelial activation in sepsis.
abstract: Near infrared spectroscopy (NIRS) may be utilized in conjunction with a vascular occlusion test to quantify a tissue bed's ability to re-oxygenate by measuring continuous tissue oxygen saturation recovery rate. We hypothesize that NIRS recovery slope will be associated with expression of endothelial biomarkers, thus, making it a feasible bedside surrogate for assessing endothelial activation/dysfunction in patients with sepsis. A secondary analysis of a prospective, multicenter, observational study was done on a convenience sample of adult patients at four university emergency departments consisting of patients with septic shock, sepsis without shock and patients without infection. At enrollment we measured the NIRS-derived measurements and collected plasma to assay biomarkers of endothelial activation. 186 patients were enrolled in the study. The mean age was 63 (± 16) years with 60 % male gender. Univariate analysis assessing the linear relationship between the recovery slope with endothelial biomarkers, found a weak but statistical significant association between NIRS recovery slope and soluble fms-like tyrosine kinase-1 (sFLT-1) and tPAI-1 (r = -0.08, p < 0.0001 and r = -0.06, p = 0.002). When adjusting for diabetes, age and sequential organ failure assessment score at enrollment, only sFLT-1 persisted having a statistically significant association (r = -0.04, p = 0.01). We found a weak, but statistically significant relationship between NIRS-derived measurements and biomarkers of endothelial activation/dysfunction in patients with sepsis. This study fails to support the use of NIRS-derived measurements as a clinical or research tool to identify patients with endothelial cell activation/dysfunction and informs researchers that this is not a robust option for identifying this lesion at the bedside.
authors.affiliation: Department of Emergency Medicine and Center for Vascular Biology Research, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA. sskibste@bidmc.harvard.edu
authors.forename: Simon
authors.initials: S
authors.lastname: Skibsted
authors.forename: Ryan
authors.initials: R
authors.lastname: Arnold
authors.forename: Robert
authors.initials: R
authors.lastname: Sherwin
authors.forename: Sam
authors.initials: S
authors.lastname: Singh
authors.forename: David
authors.initials: D
authors.lastname: Lundy
authors.forename: Teresa
authors.initials: T
authors.lastname: Nelson
authors.forename: Michael Alexander
authors.initials: MA
authors.lastname: Puskarich
authors.forename: Stephen
authors.initials: S
authors.lastname: Trzeciak
authors.forename: Alan Edward
authors.initials: AE
authors.lastname: Jones
authors.forename: Nathan Ivan
authors.initials: NI
authors.lastname: Shapiro
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006801:Humans; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000378:metabolism*; D010101:Oxygen Consumption / Q000502:physiology; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D018805:Sepsis / Q000503:physiopathology*; D012772:Shock, Septic / Q000503:physiopathology*; D019265:Spectroscopy, Near-Infrared; D018746:Systemic Inflammatory Response Syndrome / Q000503:physiopathology
chemical_list: D015415:Biomarkers; D015850:Interleukin-6; D017395:Plasminogen Activator Inhibitor 1; D010100:Oxygen